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T antigens' role in polyomavirus transformation: c-myc but not c-fos or c-jun expression is a target for middle T.
Rameh LE, Armelin MC
(1991) Oncogene 6: 1049-56
MeSH Terms: Animals, Antigens, Polyomavirus Transforming, Cell Line, Cell Transformation, Viral, DNA-Binding Proteins, Fibroblasts, Gene Expression, Mice, Mice, Inbred BALB C, Polyomavirus, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-fos, Proto-Oncogene Proteins c-jun, Proto-Oncogene Proteins c-myc, RNA, Messenger, Transcription Factors, Transfection
Show Abstract · Added November 26, 2018
Polyoma virus (Py) causes neoplastic transformation in vitro and multiple tumors in vivo. The role played by large and middle T antigens (LT, MT) and their mechanisms of action are focused here. Py-transformed Balb-3T3 cells become independent of platelet-derived growth factor (PDGF) for growth. JE, c-fos, c-jun and c-myc are 'immediate early' genes induced in response to PDGF. To test whether these cellular genes play a role in malignant transformation by Py, we generated a number of transfectant cell lines overexpressing LT, MT or both. Characterization of these cell lines revealed that: (a) MT but not LT causes morphological transformation, ability to grow in agarose suspension; (b) cooperation between LT and MT is evident in vitro, however, high and simultaneous LT and MT expression does not warrant tumorigenic potential; (c) MT expression does not correlate with tumorigenic potential but alters the probability of eliciting tumors; (d) JE and c-myc (but not c-fos or c-jun) are constitutively expressed in MT transfectants. MT induction is followed by c-myc induction 1.5 h later. We conclude that some of the 'immediate-early' genes may play pivotal roles in Py transformation.
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Translational activation of the non-AUG-initiated c-myc 1 protein at high cell densities due to methionine deprivation.
Hann SR, Sloan-Brown K, Spotts GD
(1992) Genes Dev 6: 1229-40
MeSH Terms: Amino Acid Sequence, Animals, Base Sequence, Cell Count, Codon, DNA, Gene Expression Regulation, Humans, Kinetics, Methionine, Molecular Sequence Data, Protein Biosynthesis, Proto-Oncogene Proteins c-myc, Tumor Cells, Cultured
Show Abstract · Added March 5, 2014
c-myc belongs to a small, yet growing, group of eukaryotic mRNAs that initiate translation inefficiently from a non-AUG codon upstream from a more efficient AUG codon. We have examined the translational regulation of non-AUG-initiated c-myc 1 and AUG-initiated c-myc 2 protein synthesis in avian and mouse cells during proliferation. As lymphoid, erythroid, and embryo fibroblast cells approached high densities in culture, there was a sustained 5- to 10-fold induction in the synthesis of c-myc 1 protein to levels greater than or equal to c-myc 2 protein synthesis. Treatment with conditioned/depleted media from high-density cells was able to reproduce this activation in low-density cells within 5 hr. Additional studies with the conditioned/depleted media revealed that amino acid availability, specifically methionine deprivation, was responsible for this unique translational control. Our results describe a specific and dramatic regulation of dual translational initiation. Furthermore, these results represent a novel translational activation of a specific gene in higher eukaryotes in response to nutrient deprivation.
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14 MeSH Terms